多巴胺引起的突触后长期增强（LTE）可能由钙离子和钙调蛋白介导。
Postsynaptic long-term enhancement (LTE) by dopamine may be mediated by Ca2+ and calmodulin.
作者信息
Mochida S, Libet B
机构信息
Department of Physiology, Tokyo Medical College, Japan.
出版信息
Brain Res. 1990 Apr 9;513(1):144-8. doi: 10.1016/0006-8993(90)91100-u.
Long-term enhancement (LTE), of postsynaptic slow depolarizing responses to a muscarinic agonist (MCh), follows a brief exposure of the rabbit superior cervical ganglion to another transmitter, dopamine (DA). Either reduction of external Ca2+ (to 1.0 mM or 0.2 mM) or presence of a specific calmodulin antagonist (calmidazolium at 5 microM) blocked DA induction of this LTE. However, unlike LTP in hippocampus, induction of LTE is not mediated by depolarization-dependent influx of Ca2+.
对毒蕈碱激动剂（MCh）的突触后缓慢去极化反应的长期增强（LTE），在兔颈上神经节短暂暴露于另一种递质多巴胺（DA）后出现。外部Ca2+浓度降低（至1.0 mM或0.2 mM）或存在特定的钙调蛋白拮抗剂（5 microM的氯氮卓）均可阻断DA诱导的这种LTE。然而，与海马体中的长时程增强（LTP）不同，LTE的诱导不是由去极化依赖性Ca2+内流介导的。
Zotero 插件